Stroke or ischemia is caused by a blockage in a specific blood vessel that partially or completely reduces the blood flow to the brain. Nutritional factors such as antioxidants and healthy eating patterns are important variables in preventing stroke. Molecular composition properties such as molecular binding and screening can be used to evaluate the specific activity and morphological changes. The present study aimed to evaluate the effectiveness of pharmacological correction of the consequences of a hemorrhagic stroke in rats with a new derivative of taurine magnesium-bis-(۲-aminoethanesulfonic)-butadioate. The animals (n=۱۷۰) were divided into four groups as follows: ۱) control group (n=۲۰), ۲) group ۲ suffered a hemorrhagic stroke without pharmacological correction (n=۵۰), ۳) group ۳ (n=۵۰) underwent simulation of hemorrhagic stroke received
Taurine at the dose of ۵۰ mg/kg, ۴) Group ۴ underwent simulation of hemorrhagic stroke with correction of hemorrhagic stroke with magnesium-bis-(۲-aminoethanesulfonic)-butadioate at the dose of ۱۵۰ mg/kg (LKHT ۳-۱۷) (n=۵۰).
Hemorrhagic stroke was induced by transfusing autologous blood into the parietal lobe of the right hemisphere of the brain. Lethality, neurological status, locomotor, and exploratory behavior, as well as the morphological pattern of the brain damage, were assessed on the ۱st, ۳rd, and ۷th days after the pathology simulation. Neurological deficit was determined in animals by the McGrow stroke index scale. The locomotor and exploratory behavior was evaluated using the Acti-track software and hardware complex. Two criteria were considered when assessing morphological changes in the brain: the average thickness of the cerebral cortex (in micrometers) and the number of neurons without degenerative changes. LKHT ۳-۱۷ (۱۵۰ mg/kg) and taurine (۵۰ mg/kg) reduced lethality by ۱.۷ and ۱.۳۶ times, respectively, on the ۳rd day after stroke compared to that of the control (p<۰.۰۵). In parallel, a neurological deficit was effectively corrected LKHT ۳-۱۷ and taurine to ۵.۳±۰.۸ and ۶.۵±۰.۹, respectively, on the ۱st day in contrast to the control of ۸.۱±۰.۷ points. The locomotor and exploratory behavior was significantly different on the ۷th day and was accompanied by a significant increase in total activity under the influence of LKHT ۳-۱۷ to ۴۹۱ conventional units (CU) compared to the control of ۱۱۰ conventional units. On the ۱st day, the thickness of the cortex was ۱۹۴۳.۷±۴۴.۰۸ µm, and ۱۴۹۱.۰±۳۸.۶۱ µm in the control and LKHT ۳-۱۷ groups, respectively. The number of neurons without neurodegenerative changes prevailed in LKHT ۳-۱۷ group (۱۸.۷±۴.۳۲), and the lowest number was observed in the group without pharmacological correction of the pathology (۱۴.۳±۳.۷۸). The taurine derivative magnesium-bis-(۲-aminoethanesulfonic)-butadioate, which is a combination of the amino acid, magnesium ion, and succinic acid, decreases the neurological deficits, lethality, and enhances the locomotor and exploratory behavior in experimental hemorrhagic stroke in rats. The effect of the studied medication on the dynamics of molecular pathophysiological mechanisms occurring in the cell requires additional research.